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Effect of intrananasally administered deferoxamine in the intracerebroventricular streptozotocin rat model of Alzheimer's disease

ABSTRACT: Effect of intrananasally administered deferoxamine in the intracerebroventricular streptozotocin rat model of Alzheimer's disease

PROVIDER: PRJNA1185735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31332464_1.fastq.gz	Fastqsanger.gz
	SRR31332464_2.fastq.gz	Fastqsanger.gz
	SRR31332465_1.fastq.gz	Fastqsanger.gz
	SRR31332465_2.fastq.gz	Fastqsanger.gz
	SRR31332466_1.fastq.gz	Fastqsanger.gz

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Effect of intrananasally administered deferoxamine in the intracerebroventricular streptozotocin rat model of Alzheimer's disease

Project description:Intranasal (IN) deferoxamine (DFO) has emerged over the past decade as a promising therapeutic in preclinical experiments across neurodegenerative and neurovascular diseases. As an antioxidant iron chelator, its mechanisms are multimodal, involving the binding of brain iron and the consequent engagement of several pathways to counter pathogenesis across multiple diseases. We and other research groups have shown that IN DFO rescues cognitive impairment in several rodent models of Alzheimer Disease (AD). This study was designed to probe dosing regimens to inform future clinical trials, while exploring mechanisms within the intracerebroventricular (ICV) streptozotocin (STZ) model. Using RNA-sequencing and pathway analysis, STZ was shown to induce several pathways of cell death and neuroinflammation, and IN DFO engaged multiple transcriptomic pathways involved in hippocampal neuronal survival. To our knowledge this study is the first to assess the transcriptomic pathways and mechanisms associated with either the ICV STZ model or DFO treatment, and the first to demonstrate efficacy at this low dose.

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Project description:au08-04_dfo - analysis of deferoxamine treated leaves and roots - What are the effects of the siderophore deferoxamine on Arabidopsis leaves and roots? - Plants were allowed to grow for 5-6 weeks. The nutrient solution contains 0.25 mM Ca(NO3)2.4H2O, 1mM KH2PO4, 0.5 mM KNO3, 1mM MgSO4.7H2O, 50 µM H3BO3, 19 µM MnCl2.4H2O, 10 µM ZnCl2, 1 µM CuSO4.5H2O, 0.02 µM Na2MoO4.2H2O and 50 µM FeNa-EDTA. Plants were subjected to an 8 h light/16 h dark cycle, at 19°C, with 70% relative humidity. Leaves of six week old hydroponically grown A. thaliana Col0 plants were infiltrated with 1mM deferoxamine or sterile distilled water. Leaves were harvested 7 and 24 h.p.i. Keywords: time course,treated vs untreated comparison

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Project description:Chemicals, such as MNU (N-methyl-N-nitrosourea) and NaIO3 (sodium iodate), are widely used to induce retinal degeneration in rodents. Streptozotocin (STZ) is an analog of N-acetyl glucosamine in which an MNU moiety is linked to a hexose and has a special toxic effect on insulin-producing pancreatic β-cells. It is commonly used to induce hyperglycemia to model diabetes. While intracerebroventricular injection of STZ can produce Alzheimer's disease independent of hyperglycemia, most retinal studies using STZ focus on the effects of hyperglycemia on the retina, but whether STZ has any impact on retinal cells independent of hyperglycemia is unknown. We aimed to investigate the role of cytotoxicity of STZ in rat retina. Intravitreal (5ug or 10ug) or subcutaneous (30mg/kg) injection of STZ at the early stage of newborn rats couldn’t induce hyperglycemia but caused NSIR (neonatal STZ-induced retinopathy), including reduced ERG amplitudes, retinal rosettes and apoptosis, cell cycle arrest, microglial activation, and delayed retinal angiogenesis. STZ did not affect the early-born retinal cell types but significantly reduced the late-born ones. Short-term and long-term hyperglycemia had no significant effects on the NSIR phenotypes. RNA sequencing revealed that STZ induces oxidative stress and activates the p53 pathway of retinal cells. Locally or systemically, STZ injection after P8 couldn’t induce NSIR when all retinal progenitors exit the cell cycle. Thus, NSIR in rats is independent of hyperglycemia but due to STZ’s direct cytotoxic effects on retinal progenitor cells. NSIR is a typical reaction to STZ-induced retinal oxidative stress and DNA damage. This significant finding suggests that NSIR may be a valuable model for studying retinal progenitor DNA damage-related diseases, potentially leading to new insights and treatments.

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